Natremia – Concentration of sodium of plasma, normal range is 135 / 145 mmol/l
hypernatremia – Higher plasmatic concentration of sodium, the most common developed because of free water looses
hyponatremia – Lowered plasmatic concentration of sodium, developed mostly because of free water retention
Aldosterone – Hormone of adrenal cortex controlled by RAAS (renin- angiotensin-aldosteron system), increases sodium and water resorption and simultaneously potassium excretion in kidneys
Atrial natriuretic factor – ANF (NAF, ANP) peptide which protects heart from overload by volume. Its secretion raises when there is increased pressure to walls of right ventricle and oneself leads to excretion of water and sodium in proximal and distal renal tubuli.
kalemia – Concentration of potassium in plasma with normal range of 3,5 – 5 mmol/l
hyperkalemia – Increased plasmatic concentration of potassium (above 5 mmol/l)
hypokalémie – Decreased plasmatic concentration of potassium (bellow 3,5 mmol/l)
calcemia – Concentration of calcium in plasma with normal range of 2 – 2,75 mmol/l. One half of this measured level of calcium in normal conditions is present as in the bounded non-diffusible form and second one in the free diffusible form. This balance can be influenced by presence of other polar particles in plasma which also influence pH.
hypercalcemia – Increased plasmatic concentration of calcium.
hypocalcemia – Decreased plasmatic concentration of calcium.
Ionised calcium – Unbound free calcium ions in the biologic active form of Ca2+, participates on the coagulation, influences cellular activity. Increased extracellular concentration stabilises membranes but in the other hand increased intracellular concentration leads to higher irritability.
Bounded Calcium – Calcium in plasma bounded to proteins. Ratio of bounded and free calcium depends highly on pH of plasma, which is impact of ionised particles presence.
calcification – Accumulation of calcium salts in tissues.
Cholekalciferol – Precursor of calcitriol activated by UVB radiation.
Calcitriol – Vitamin D activated in the livers and kidneys to 200 times more active hormone.
ergocalciferol – Precursor of calcitriol obtained in nourishment.
Parathyroid hormone – PTH
parathormon related protein – PTH rp secerned by some malignant tumours, it has similar effect as PTH
paresthesia – Sign of increased irritability, sensation of unreal tingling.
tetany – Increased neuromuscular irritability. Generates parestesiae like a tingling of fingers or tongue and even painful involuntary muscle spasms mostly of small muscles of limbs (e.g. carpopedal spasms).
carpopedal spasms – Concrete form of tetanic spasms of acral parts of limbs caused by deficiency of ionised calcium in plasma. Small motor units of acral muscles are very sensitive to calcium concentration and thus reacts first.
2. Sodium Bilance
Sodium (Na+) is the major cation of extracellular fluid (ECF), its plasma concentration is about 135 – 145 mmol / l. The organism gets with food in the form of table salt. The recommended daily intake is 2 g / 24 hours, but daily intake in the population of central Europe is around 5 g / 24 hours. Sodium is absorbed in the middle and distal parts of small intestine, in the large intestine is its absorption controlled by aldosterone. Sodium cations are always accompanied by water, and thus contributes these ions to thickening digesta. Sodium excreted out of organism by urine and sweat. Determinant influence on the balance have kidneys. From the primary urine approximately 85% of the sodium absorbs back to the circulation in the proximal channel, about 14.5% in the distal channel and only 0.5% is excreted by kidneys as a part of urine.
The importance of sodium is in maintaining of circulating volume in cardiovascular bed and in preserving of total somatic water. The volume of the circulating fluid is essential for maintaining blood pressure, that’s why sodium control is linked to vegetative nervous system and can activate the stress response. Sodium counts on 80% of plasmatic osmolarity and is very important for action potential equilibrium of cells.
2.1 Control of sodium homeostasis
Water and sodium are closely interconnected. The basis of their homeostasis is an active transport of sodium, which is followed by water according to osmotic gradient. Sodium is a positively charged ion passing between compartments together with chloride anions to keep electrochemical balance.
There are chemoreceptors monitoring the concentration of sodium and chloride ions in juxtaglomerular apparatus. Decreased concentration of those two ions irritates those chemoreceptors and lead to higher secretion of hormone Renin. The renin – angiotensin – aldosterone system (RAAS) is then activated., We know that this axis is activated also by decreased blood flow through the kidneys (baroreceptors monitor the pressure of blood which circulates through jaxtaglomerullar apparatus too) from the previous chapter. Activation of mentioned RAAS axis leads to reabsorption of sodium in distal tubules and collecting ducts. Water is passively reabsorbed together with sodium. Total amount of sodium in body then increases, but its concentration doesn’t changes (ratio of sodium – water is the same). Aldosterone leads to excretion of protons too, this loss of hydrogen can evolve into hypokalemia and metabolic alkalosis.
In the juxtaglomerular apparatus are chemoreceptors, which monitor the concentration of sodium and chloride ions and according to their stimulation decrease secretion of renin. This way is activated so called axis Renin – Angiotensin – Aldosterone Axis (RAAS – Renin – Angiotensin – Aldosteron System). We know from the previous chapter that this axis is activated also by decreased blood flow through the kidneys (baroreceptors monitor the pressure of blood flowing through the juxtaglomerulárním apparatus). RAAS axis activation leads to reabsorbtion of sodium thanks to the effect of aldosterone at distal tubules and collecting duct. Water is reabsorbed passively with sodium. This will increase the amount of sodium in the body, but it will not increase its concentration in body fluids (ratio of sodium – water is retained). Aldosterone action also leads to excretion of hydrogen ions (equal protons) in the distal tubule and protons, thus increase of aldosteron may cause hypokalemia and metabolic alkalosis.
During the increasing of volume in the right atrium increases the pressure in the right atrium and atrial natriuretic factor (ANF) excretion evolves. ANF facilitates the excretion of sodium with the water passively in both proximal and distal tubules of the kidney and collecting ducts. The ratio of sodium: water is maintained again, the amount of sodium in the body is so reduced, but concentration does not change. This fact can be used to observate the plasma levels of ANF as a marker of cardiac activity for example during accumulation of blood in the circulation before right ventricle when the patient suffers by pathologic condition called the right heart failure.
Sodium concentration in the plasma may change when there are changes in plasma free water content. Sodium cations are diluted and their concentration is reduced when there is increase in the amount of water, during reduction of the water ammount the concentration of sodium increases on the contrary. The total content of sodium in the body does not change. The mechanism of changing the balance of free water is influenced by the antidiuretic hormone – ADH. However change of the sodium concentration also accompanies states of altered hydration. During acute dehydration there is relative increase in the sodium concentration, during overhydration the sodium concentration decreases.
Estimate of changes in water volume of the patient's body fluids and the sodium concentration in the plasma according to patient's weight: x (l) = m . 0,6 . (1 – [Na+] /140) kde: x ….. loss (overload)of water in litres m….. patient's weight 0,6…. proportional part of patient's weight constituted by water (ICF + ECF = 60%) [Na+] .. plasmatic sodium concentration
2.2 Disturbances of sodium
Hyponatremia means decreased sodium concentrationin plasma (below 135 mmol / l). It is one of the most common ionic equilibrium disturbances in hospitalized patients. Frequent cause of this state is some reduction in sodium concentration on the basis of free water resorption as a consequence of elevated ADH secretion which evolves during a decrease of volume in circulation (fluid loss), or during an increased osmolarity of plasma (hyperglycemia). Hyponatremia is sometimes based on intracellular hypokalaemia, which changes the concentrations of ions and water in the body (during loss of IC potassium IC osmolarity reduces and follows transfer of water from a low osmolarity space (IC) to higher osmolarity space (EC). Hyponatremia can be also established even when the total amount of sodium in the body is increased, but deteminative storage of sodium is outside of the plasma (such as swelling during right heart failure or in patients with water retention of renal basis). Compensatory mechanisms tend to increase water retention (through aldosterone and ADH) and the sodium concentration is afterward reduced. Sodium stored in the swelling has significantly slower dynamics than sodium in the plasma (sodium concentration changes in swelling is slower than in the blood circulation and remains the same for some time during rapid decrease of concentration in the plasma). Hyponatremia can accompany dehydration, overhydration and normal hydration.
Tab. IV.1 Causations of hyponatremia
|primary secretion of ADH||Retention of free water, “dilutional” hyponatremia||SIADH (syndrome of inappropriate ADH secretion)
in eldery (rise of ADH basal secretion)
other states of increased osmolarity of ECT
| secretion of ADH as reaction to osmolarity||Bad compensation od diabetes mellitus or other|
|change in hydratation|| secretion of ADH as reaction to decreased volume of ECF (through stimulation of sympathetic part of vegetative nervous system)||krvácení, popáleniny, průjmy, zvracení, excesivní pocení|
|Dilution by low sodium water intake||Destilated water drinking
Drawning in the fresh water
|Decrease of IC potassium concentration||Establishing of new somotic equilibrium of IC and EC space – water shifts according to concentration gradient||Diabetes mellitus
|Swelling||Losses of water and sodium to the storage in interstitial space
Compensation of decreased intravasal volume by ADH
|Body swelling eg. During right heart failure|
Symptoms of hyponatremia depend on the magnitude of hyponatremia and the speed of its development. Symptoms are caused mainly by changing the function of tissues, which are sensitive to changes in osmolarity and thus changes in cell volume – e.g. CNS cells, that’s because sodium creates significant part of osmolarity in organism. Imbalance of intracellular and extracellular osmolarity leads to the transfer of water into cells and thus to intracellular oedema, which disturbs neural cells function in the brain at first (even small changes). Headaches, impaired concentration and disturbances of consciousness evolve. Brain tissue adapts to developing hyponatremia by the reduction of osmolarity reducing ion content in the interstitium (in up to 24 hours) and organic osmotically active substances in cells of CNS (in about 48 hours). Although this mechanism reduces intracellular edema of the brain, there emerges risk of permanent brain damage by dehydratation if there will be too rapid therapy of hyponatraemia. Cells need time to restore amount of effective intracellular osmotic solutes. Replenishment of ions and organic particles is slower than its reduction when the disturbance occurs (ions are renewed in tens of hours, the organic solutes in many days).
Hypernatremia is a condition in which sodium concentration in plasma is bigger than 145 mmol/l. At a concentration of about 155 mmol / l there is risk of death. Hypernatremia always leads to hyperosmolarity and thereby to compensational increase of ADH and to following water retention.
Hypernatremia can be caused by a loss of water from the ECF (hypoosmolar fluid loss eg. as during the free water losses in diabetes insipidus, diarrhea, sweating or by sticking out of gastric contents through probe). Hypernatremia can be induced by both hyperosmolar solutions or excessive salt intakes. Hyponatremia can be associated with overhydration, dehydration and normal hydration likewise above.
Symptoms of hypernatremia are again neurologic and induced by the shift of water out of brain cells according to concentration gradient because of increase in plasmatic osmolarity. Similarly brain can adapt to hyponatremia during the slow change . Rapid adjustment of this state by therapy can lead therefore to brain swelling too.
3 Potassium balance
Potassium (K+) is the major intracellular cation. Its concentration in the extracellular (EC) fluid is maintained at a relatively low level. The main function of EC potassium is to maintain the resting membrane potential. The membrane potential depends on the ratio of intracellular to extracellular concentrations of potassium cations. Any change in the extracellular potassium concentration leads to a change of membrane potential which determines cellular functions. Cells are very sensitive to potassium balance so even small changes in the concentration of the EC potassium lead to large consequences. Potassium concentration in the plasma is mostly an indicator of cell membrane excitability than marker of potassium reserves in the body but it can be used as indicator of pH and it can be lethal when presented in extreme values out of the normal range.
95% of potassium is intracellular [150 mmol/l]. In ECF is concentration between 3,5 – 5,0 mmol/l. ICF/ECF gradient K+ is maintained by electrochemic activity and leads to equilibrium on the cellular membrane, Na+/K+ pump equalizes by active transport changes induced by action potential and other phenomena.
OBR. VI.1: NA+/ K+ PUMP
K + intake is regulated (controlled). Potassium comes into the body from food, it presents eg. in fruits (apricots, bananas) and meat. After intake of bigger amount of potassium is the major part of about 80% transported from blood into cells thanks to the action of insulin which activates the Na + / K + pump – so called Na-K-ATPase), from there it is slowly released and gradually excreted in urine (cells are preventing an abrupt increase potassium of potassium in blood after food intake, they actually buffer it) . Kidney excrete in 4 hours about 50% of ingested potassium.
K + moves from cell to cell depending on two mechanisms. At first according to the activity of the Na + / K + pump (Na / K ATPase) and at second based on pH in the extracellular space.
Na+/K+ pump draws potassium against cellular concentration gradient in ratio of 3 sodium ions going out of the cell and 2 potassium ions inside. Activity of pump is induced by:
Increased concentration of K+ in extracellular fluid (ECF)
Adrenaline (epinephrine): b2-receptors stimulate Na-K-ATPase, a2-receptors inhibit it to the contrary
During changes of acid-base equilibrium cells involve in the buffering of hydrogen cation contra potassium cation.
When there is lower amount of hydrogen cations in the ECF, that means in alkalosis there is outflow H+ outside of cells and on the contrary K + enters cells (according to electrochemical gradien, if positive ion go out of the cell, then is missed and got to be substituted by another one), there is hypokalaemia.
When there is excess of hydrogen cations in the ECF, that means in acidosis enters H+ ion the cell and K+ outflows to maintain electrochemical balance of the cell. Thus during acidosis evolves hyperkalemia.
Because of mentioned phanomena everybody has to always evaluate potassium concentration in plasma (serum potassium) in relation to the pH. When during acidosis occurs hypokalaemia, there have to be necessarily at least two different processes together leading to this presentation, as well as when hyperkalaemia appears during alkalosis).
The excretion of potassium out of body is dividet between kidneys making major part of outflow of about 90% and the digestive tract providing the rest of 10%. Secondary urine excretion of potassium depends primarily on K + secretion in the distal tubules and collecting ducts. In kidneys is potassium freely filtered by the glomeruli, it gets into the primary urine in the proximal tubules and Henle’s twist, then it is all absorbed back from the lumen. Aldosterone afterwards induces in the distal tubule and collecting duct excretion of potassium to the lumen according to organisms needs. Polyuria increases from the certain point excretion of potassium and leads to hypokalaemia, while oliguria and anuria lead to hyperkalemia. Same mechanism is influenced by some drugs.
Tubular secretion is modified following factors:
Aldosterone increases the activity of the Na + / K + pump. Potassium is pumped against the concentration gradient into cells of tubules and thereby is increased the electric gradient between cells and tubules. Potassium can then easily flow after the electrochemical gradient into the tubule and is transported with tubular fluid.
Kortisol in high doses have the same effect as aldosterone.
Tubular fluids flow speed, because faster flow washes out potassium present in tubule, this mechanism maintains gradient between cells and lumen and thus potentiate transport of potassium from cells to lumen and to secondary urine.
Increased extracellular concentration of K+, since potassium presence enhances transfer into tubular cells (as well as to every other cell) and by this way increases the gradient for the transition of K+ into the lumen of the tubule too.
Extracellular pH: hydrogen ions go out of cells during alkalosis (this mechanism is equivalent for all of body cells including tubular cells) and K+ ions from the outer space go into cells to compensate this loss of indoor protons. This will increase the concentration gradient of potassium and enhance the excretion of potassium into the lumen. Acute alkalosis increased secretion of K+ (leading to hypokalemia). Acute acidosis leads by the opposite mechanism to the K+ secretion leads and hyperkalemia.
Physiological way to loose potassium physioligally through the digestive tract is excretion in the faeces (chyme is in colon maked furthermore thicker thanks to the action of aldosterone, which helps to absorb sodium and water from the colons lumen and to excrete potassium into the lumen). Potassium can be lost from the body during pathologic conditions like diarrhea and vomiting.
3.1 Disturbances of potassium concentration
Hyperkalemia is defined as the potassium concentration in plasma greater than 5 mmol/l. This may be due to increase in the total amount of potassium in the body after increased intake of food, but in a healthy young person is in most cases higher potassium intake compensated by the aforementioned mechanism, which ensures the temporary removal potassium into cells.
The hyperkalemia can result also in:
Rapid administration of a K+ in infusion (therefore is always added glucose and insulin in order to accelerate the transfer to cells, when therapy requiring rapid intake of K+ is demanded)
transfusion of older blood (with following decay of erythrocytes containing potassium)
Reduced kidney function: decreased renal perfusion (eg. in dehydration), acute renal failure, inadequate secretion of aldosterone (Addison’s disease), use of potassium-sparing diuretics.
Another cause can be the shift of potassium from cells to the ECF, which is the most common cause of acute hyperkalemia in:
Tissues breakdown: muscle tissue (so called rhabdomyolysis) eg. after excessive stress on organism like during and after marathon run
Cellular necrosis due to ischemy, inflammation or during breakdown of tummor
Hemolysis or bleeding to the gastrointestinal tract
Insufficiency of insulin
Consequences of hyperkalemia leads mainly to change of irritability of muscle cells, neurons and to change of acid base equilibrium.
Change in excitability of neural and muscle cells. Resting membrane potential moves due to an excess of positive potassium in a positive direction, ie. it becomes less negative, so the cell becomes more irritable:
During the first phase of hyperkalemia it is easier to trigger the activation of voltage-gated channels of cellular membrane. Resting membrane potential of -90 mV approaches the value of minus 65 mV, when this in positive manner higher value is reached voltage-gated Na+ channels open, these channels are in first line responsible for the generation of the membrane depolarization. Hyperkalemia therefore increases excitability and conductivity, arrhythmias can develop in heart and patients can have paresthesias.
If is hyperkalemia such extreme that the resting membrane potential reaches minus 65 mV in the most of body cells, then sodium channels became inactivated and the second phase starts. Typical spectrum of symptoms there is from the muscle weakness to paralysis.
Change of acid-basis equilibrium. Potassium enters cells mainly because of Na+/K+ pump activation and hydrogen goes out of cells to compensate and maintain electrochemical equilibrium. Methabolic acidosis evolves.
Mentioned changes influence the whole organism but most obvious consequences are presented through the cardiovascular system.
Disturbances of the cardiac rhythm
Change of the myocardial excitability causes futher changes on ECG:
At first T wave raises, spiky T wave shows because of fasterrepolarisation of ventricles (see the curve A on the picture 4.2)
P wave decreases (also curve A picture 4.2)
QRS complex widens because of slowering of depolarisation caused by a group of sodium channels which could not be activated and so can not involve in depolarisation (see curves B to E on the picture 4.2)
The curve progredes to the sinusoidal shape (see curves D and E on the picture 4.2)
Decrease of the blood pressure because of vasodilatation. Potassium is one of local factors regulating vessel tonus.
Compensation options: Elevated levels of potassium induce secretion of aldosterone. This step begins with hyperpolarization of the membrane secretory cells due to the presence of potassium, shift leads to an increased activation of the secretion of aldosteron in the adrenal cortex and mentioned hormone subsequently increases potassium excretion by the kidneys.
Therapy options: Increased concentration of calcium in extracellular space stabilizes membrane of every cell and reduces therefore excitability. When there are just slightly elevated potassium levels in ECF we can stabilisate excitability of cellular membranes by intravenous administration of extracellular calcium, this stabilisation reduces at first hyperexcitability of the myocardium. If the patient has functioning kidney, we can administer potassium wasting diuretics, which increase the excretion of potassium, but should always be considered together with the cause of this condition and used as a treatment just if it is beneficial for the patients future, otherwise they can be harming. If it is necessary to arrange an extra time for the preparation of dialysis in case of kidney failure, we can administer additional insulin with glucose, this combination increases the transfer of K+ into the cells. We can also give to patient NaHCO3. Sodium activates the Na+/K+– ATPase, thereby increasing the transfer of potassium into the cells and bicarbonate presence supports this transfer by the establishing of alkaline environment. The effect lasts about 30 minutes In both mentioned cases. The last option for managing the kidney failure is dialysis.
Hypokalemia evolves frequently after reducing the total amount of K+ in the body, but may be rarely caused by transfer of K+ into the cells too. Symptoms become to be apparent at concentrations below 3 mmol/L.
Real potassium deficiency can be caused by following.
Reduced intake, like during starvation, anorexia and alcoholism
Lowered circulating volume, for example after profused sweating, diarrhea, loss of fluids through gastrointestinal fistulas. Subsequently, the water losses are compensated by RAAS activation and increased potassium excretion in the urine, or even by secretion of ADH and diluting the plasma.
Vomiting which causes more mechanisms. There may be a direct loss of K +, there can be induction of alkalosis by loss of protons and chlorides which leads to the transfer of K+ into the cells. Water loss induces aldosterone secretion, presence of this hormone leads to increase of K+ excretion by the kidney. Final state is often produced by combination of mentioned mechanisms.
Decrease in the resorption of K + at the intestine during diseases of the intestinal wall.
Loss through kidneys, as the action of diuretics, by aldosterone hypersecretion or presence of bigger load of corticosteroids.
Polyuria of any cause, e.g. during hyperglycemia, as it induces potassium excretion in the kidneys.
Relative potassium deficiency origins in shift of potassium into cells:
During acute alkalosis.
By increased insulin concentration (insulin activates Na+/K+ pumpu).
After administration of beta-adrenergic agonists (activation of Na+/K+ pump).
Hypokalemia is the most common ion imbalance in clinical field. Fifth of hospitalized patients has a value of less than 3.6 mmol / l and a quarter of those patients has values of less than 3 mmol / l. Hypokalaemia is measured in 10-40% of ambulant patients. Hypokalemia is there often found coincidentally during laboratory tests ordained for another reason.
Consequences of hypokalemia:
Change in membrane potential of nerve and muscle cells: so called hyperpolarization occurs when membrane potential becomes more negative and thus there have to be more potent stimuli to elicit responses. Muscle weakness to paralysis evolves and scretion of some endocrine cells can be altered, e.g. aldosterone and insulin secretion decreases.
Cardiovascular system: conduction of action potential elongates and automaticity of the heart reduces. Rhythm disturbances at the heart arise, T-wave on ECG is reduced and wave U may show.
Structural changes: chronic potassium deficiency leads to fibrosis of muscle cells and to vacuolation of distal tubules in the kidneys which causes a reduction in the sensitivity to ADH (nephrogenic diabetes insipidus arises).
Compensation: potassium deficiency changes polarity of beta cells membranes in the pancreas and reduces insulin secretion leading to compensatory decreased shift of K+ into cells caused by decreased insulin, very important consequence is raising blood glucose. The same mechanism causes reduction in aldosterone secretion in the adrenal cortex and leads to decreased potassium excretion by the kidneys.
Treatment: oral potassium if necessary. Potassium is generally administered with insulin (which reinforces the change of potassium into the cells) to avoid transient hyperkalemia with heart rhythm disurbances and hypoglycemia.
4 Balance of calcium
The function of calcium (Ca2+) in the body:
Essential building component of bone and tooth tissue.
Allows muscle contraction (in skeletal muscle contraction comes from intracellular sources of sarcoplasmic reticulum too).
Is very important for normal heart function responsible for the contraction. Myocardium requires the release of calcium from the sarcoplasmic reticulum calcium IC supplies calcium ions from the extracellular environment, it can be said that the contraction of the myocardium depends on the concentration of serum calcium.
An essential part of the blood clotting cascade so called coagulation cascade.
Acts as a second messenger in the cytosol of cells mediating some effects of hormones that have receptors on the membrane.
Activate a large number of enzymes.
Regulates nervous excitability. Increased extracellular concentration stabilizes membrane and reduces the excitability of cells, raise of intracellular calcium contrarywise increases the excitability of the cells.
After change in plasma concentration of ionized calcium the first step leads to changing excitability of most cells.
The total calcium in the body is 30 mol (1200 g) of which 75% is stored in the bones. The concentration of plasma calcium (calcemia) is 2- 2,75 mmol/l. 50% of this plasma calcium is ionised, 40-45% is bound to proteins and another part occurs in a complex with acid parts of particles. Calcium is thus present in three forms:
Ionized which is biologically active and is able to diffuse across biological membranes.
Bound to proteins which is not freely diffusible.
Complex bound as bicarbonate, phosphate or calcium citrate.
For myocardium and neuromuscular excitability is important mainly ionized calcium. Decrease in the concentration of ionized calcium in the plasma results in higher excitability.
The ratio of bound contra ionized calcium depends on the amount of protein in the plasma because increased plasma protein bounds larger amount of ionized calcium and reduces ionized part of the ratio. It also depends on the pH of the blood: Proteins are involved in buffering of blood during acidosis, they attach part of H+ but before this they have to release attached Ca+. This will increase the concentration of free calcium and reduce irritability of membranes. On the contrary when there is alkalosis protein-bound hydrogen ions are released to help maintaining acid-base balance and then ionized calcium can bound. The concentration of ionized calcium decreases during alkalosis and excitability of membranes increases as a result.
Body intake of calcium is managed through nourishment like a milk, milk products, poppy etc. It is absorbed in the duodenum and jejunum in the presence of vitamin D (calcitriol). Calcium from milk is absorbed easier, fat or excess of phosphate in the diet reduces its absorption. The daily requirement of calcium is 800 – 1000 mg, for example in 500 ml of milk there is 500 mg of Ca2+.
Regulation of calcium concentration in plasma and its amount in tissues is closely linked with the regulation of phosphate and is provided by action of parathyroid hormone, calcitriol and calcitonin. Supportive importance for this task have thyroxine which increases bone resorption together with calcium excretion by the kidneyss and cortisol which reduces the absorption of Ca2+ in the intestine and reduces the metabolism of vitamin D in the liver.
Excretion of calcium occurs mainly via the kidneys in close connection with the metabolism of phosphate, and by sweat (200-300 mg / day) and gastrointestinal tract.